Abstract
BackgroundMating changes the mode of action of 17beta-estradiol (E2) to accelerate oviductal egg transport from a nongenomic to a genomic mode, although in both pathways estrogen receptors (ER) are required. This change was designated as intracellular path shifting (IPS).MethodsHerein, we examined the subcellular distribution of ESR1 and ESR2 (formerly known as ER-alpha and ER-beta) in oviductal epithelial cells of rats on day 1 of cycle (C1) or pregnancy (P1) using immunoelectron microscopy for ESR1 and ESR2. The effect of mating on intraoviductal ESR1 or ESR2 signaling was then explored comparing the expression of E2-target genes c-fos, brain creatine kinase (Ckb) and calbindin 9 kDa (s100g) in rats on C1 or P1 treated with selective agonists for ESR1 (PPT) or ESR2 (DPN). The effect of ER agonists on egg transport was also evaluated on C1 or P1 rats.ResultsReceptor immunoreactivity was associated with the nucleus, cytoplasm and plasma membrane of the epithelial cells. Mating affected the subcellular distribution of both receptors as well as the response to E2. In C1 and P1 rats, PPT increased Ckb while both agonists increased c-fos. DPN increased Ckb and s100g only in C1 and P1 rats, respectively. PPT accelerated egg transport in both groups and DPN accelerated egg transport only in C1 rats.ConclusionEstrogen receptors present a subcellular distribution compatible with E2 genomic and nongenomic signaling in the oviductal epithelial cells of C1 and P1 although IPS occurs independently of changes in the distribution of ESR1 and ESR2 in the oviductal epithelial cells. Mating affected intraoviductal ER-signaling and induced loss of functional involvement of ESR2 on E2-induced accelerated egg transport. These findings reveal a profound influence on the ER signaling pathways exerted by mating in the oviduct.
Highlights
Mating changes the mode of action of 17beta-estradiol (E2) to accelerate oviductal egg transport from a nongenomic to a genomic mode, in both pathways estrogen receptors (ER) are required
Further investigation has shown that activity of the enzyme Catechol-O-Methyltransferase (COMT) is higher in the oviduct of cyclic than pregnant rats while OR486 a selective inhibitor of COMT blocked the effect of E2 on oviductal egg transport only in cyclic rats suggesting that decreased activity of oviductal COMT induced by mating is one of the underlying mechanisms of intracellular path shifting (IPS) [9]
We have found that levels of ESR1 and ESR2 mRNA and protein in oviducts of pregnant rats were similar to those oviducts of cycling rats, suggesting that IPS is not explained by changes in the expression of ER in the oviduct [12]
Summary
Mating changes the mode of action of 17beta-estradiol (E2) to accelerate oviductal egg transport from a nongenomic to a genomic mode, in both pathways estrogen receptors (ER) are required. This change was designated as intracellular path shifting (IPS). We demonstrated that inhibitors of RNA and protein synthesis block E2-induced oviductal embryo transport acceleration in pregnant rats, but fail to do so in cyclic rats [4,5]. E2 accelerates oviductal egg transport through nongenomic pathways in cyclic rats, while it does it through genomic pathways in pregnant rats This change in pathways has been designated "intracellular path shifting" (IPS) [9]. The physiological relevance of IPS has not been clearly established it is probable that decrease in the COMT activity induced by mating in the oviduct protects the embryos from the deleterious effect that methoxyestradiols exert during the first stages of development [10]
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